Tandem repeats and morphological variation

Blogging on Peer-Reviewed Research
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All of us mammals have pretty much the same set of genes, yet obviously there have to be some significant differences to differentiate a man from a mouse. What we currently think is a major source of morphological diversity is in the cis regulatory regions; that is, stretches of DNA outside the actual coding region of the gene that are responsible for switching the gene on and off. We might all have hair, but where we differ is when and where mice and men grow it on their bodies, and that is under the control of these regulatory elements.

A new paper by Fondon and Garner suggests that there is another source of variation between individuals: tandem repeats. Tandem repeats are short lengths of DNA that are repeated multiple times within a gene, anywhere from a handful of copies to more than a hundred. They are also called VNTRs, or variable number tandem repeats, because different individuals within a population may have different numbers of repeats. These VNTRs are relatively easy to detect with molecular tools, and we know that populations (humans included) may carry a large reservoir of different numbers of repeats, but what exactly the differences do has never been clear. One person might carry 3 tandem repeats in a particular gene, while her neighbor might bear 15, with no obvious differences between them that can be traced to that particular gene. So the question is what, if anything, does having a different number of tandem repeats do to an organism?

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Luskin on gene duplication

Casey Luskin has to be a bit of an embarrassment to the IDists…at least, he would be, if the IDists had anyone competent with whom to compare him. I tore down a previous example of Luskin’s incompetence at genetics, and now he’s gone and done it again. He complains about an article by Richard Dawkins that explains how gene duplication and divergence are processes that lead to the evolution of new information in the genome. Luskin, who I suspect has never taken a single biology class in his life, thinks he can rebut the story. He fails miserably in everything except revealing his own ignorance.

It’s quite a long-winded piece of blithering nonsense, so I’m going to focus on just three objections.

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Brains feeling stretched…

Cosma has to go and show off with a magisterial demonstration of why he is the smartest man on the internet: he’s written an exceptionally thorough description of heritability and IQ. It’s not a light read (statistics and genetics!), but it’s probably the most informative thing I’ve read in a month or more.

I’m sure I’m going to have to read it a few more times before I’ve absorbed it all.

The Hox code

Blogging on Peer-Reviewed Research

The Hox genes are a set of transcription factors that exhibit an unusual property: they provide a glimpse of one way that gene expression is translated into metazoan morphology. For the most part, the genome seems to be a welter of various genes scattered about almost randomly, with no order present in their arrangement on a chromosome — the order only becomes apparent in their expression through the process of development. The Hox genes, on the other hand, seem like an island of comprehensible structure. These are all genes that specify segment identity — whether a segment of the embryo should form part of the head, thorax, or abdomen, for instance — and they’re all clustered together in one (usually) tidy spot.

Within that cluster, we see further evidence of order. Look at just the Drosophila part of the diagram below: there are 8 Hox genes in a row, and their order within that row reflects the order of expression in the fly body. On the left or 3′ end of the DNA strand, lab (labial) is expressed in the head, while Abd-B (Abdominal-B) is expressed at the end of the abdomen.

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Schematic of relationship between Drosophila and mouse Hox genes. Hox genes are shown as colored boxes in their order on the chromosome. Orthologous genes between Drosophila and mouse, and paralogous mouse genes are shown color-coded.

Knocking out individual Hox genes in the fly causes homeotic transformations — one body part develops into another. These genes are early actors in the cascade of interactions that enable the development of morphologically distinct regions in a segmented animal — the activation of a Hox gene from the 3′ end is one of the earliest triggers that leads the segment to develop into part of the head.

Now look at the mouse part of the diagram above. We vertebrates have Hox genes that are homologous to the fly Hox genes, and they’re also clustered in discrete locations with 3’→5′ order reflecting anterior→posterior order of expression. There are differences — the two most obvious that we have more Hox genes on the 5′ side (these correspond to expression in the tail—flies do not have anything homologous to the chordate tail), and vertebrates also have four banks of Hox genes, HoxA, HoxB, HoxC, and HoxD. This complicates matters. Vertebrates have these parallel, overlapping sets of Hox genes, which suggests that morphology could be a product of a combinatorial expression of the genes in the four Hox clusters: there could be a Hox code, where identity can be defined with more gradations by mixing up the bounds of expression of each of the genes.

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FunGenEvoDevo

I got some email today with lots of constructive suggestions (See? Not all my email is evil!) for how we ought to change the education of biology students — such as by giving them a foundation in the history and philosophy of our science, using creationist arguments as bad examples so the students can see the errors for themselves, etc. — and it was absolutely brilliant, even the parts where he disagreed with some things I’d written before. Best email ever!

Of course, what helped is that I spent my summer “vacation” putting together a new freshman first semester course for biology majors that I’m teaching for the first time right now, and it’s exactly the course he described. It was eerie, like one of my future students had invented a time machine and come back into the past to tell me what to do. A lot of the course content is locked up behind a password-protected firewall, I’m afraid, but just to show you what I’m talking about, I’ll put the course schedule below the fold.

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Your mama’s soul doesn’t love you

If it existed, it might also be profoundly autistic and … diabetic? So science cannot disprove the existence of a soul, but one thing we’re learning is how much valued human properties such as love and attachment and awareness of others are a product of our biology — emotions like love are an outcome of chemistry, and can’t be separated from our meaty natures.

The latest issue of BioEssays has an excellent review of the role of the hormone oxytocin in regulating behaviors. It highlights how much biochemistry is a determinant of what we regard as virtues.

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Common elements of eumetazoan gene organization in an anemone

We now have a draft of the sea anemone genome, and it is revealing tantalizing details of metazoan evolution. The subject is the starlet anemone, Nematostella vectensis, a beautiful little animal that is also an up-and-coming star of developmental biology research.

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Nematostella development. a. unfertilized egg (~200 micron diameter) with sperm head; b. early cleavage stage; c. blastula; d. gastrula; e. planula; f. juvenile polyp; g. adult stained with DAPI to show nematocysts with a zoom in on the tentacle in the inset; h, i. confocal images of a tentacle bud stage and a gastrula respectively showing nuclei (red) and actin (green); j. a gastrula showing snail mRNA(purple) in the endoderm and forkhead mRNA (red) in the pharynx and endoderm; k. a gastrula showing Anthox8 mRNA expression; l. an adult Nematostella.

A most important reason for this work is that the anemone Nematostella is a distant relative of many of the animals that have already been sequenced, and so provides an essential perspective on the evolutionary changes that we observe in those other organisms. Comparison of its genome with that of other metazoans is helping us decipher the likely genetic organization of the last common ancestor of all animals.

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Mrs Tilton is back…forever!

She’s fired up the The Sixth International again, and she threatens promises to be at it for a long, long, long time—she bears a longevity mutation, a single nucleotide substitution in the mitochondrial genome associated with some long-lived people. And some people claim there is no such thing as a beneficial mutation…

Anyway, it’s personally interesting that it’s mitochondrial—that means it is passed down through the maternal line. Since my father’s side of the family is grievously short-lived, but my mother’s side keeps going for nearly forever, that’s good news, if the maternal secret is particularly robust mitochondria. Since this particular allele appears in various lines all around the world, there’s a slim chance.

Otherwise, I’m afraid my only mutant power seems to be the ability to dissolve chewing gum. I was ripped off.